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Periodontal Health and Diabetes
Strong evidence suggests that, unlike the conditions discussed above, diabetes is a risk factor for the prevalence and severity of gingivitis and periodontitis. Diabetes is associated with increased gingival inflammation in response to bacterial plaque, but the degree of glycemic control is an important variable in this relationship. In general, well-controlled diabetic individuals and nondiabetic people have similar degrees of gingivitis, with the same level of plaque. Conversely, poorly controlled diabetic subjects have significantly increased gingivitis, compared to either well-controlled diabetic or nondiabetic individuals.
Diabetes Mellitus and Oral Diseases
Diabetes Introduction
Diabetes Epidemiology and classification
Diabetes Pathophysiology
Clinical Presentation, Laboratory findings, and Diagnosis
Diabetes Complications
Diabetes Management
L Introduction
L Oral Agents
L Insulin
Oral Diseases and Diabetes
Periodontal Health and Diabetes
Dental Management of the Diabetic Patient
Conclusion
References
In large epidemiologic studies, diabetes has been shown to significantly increase the risk of attachment loss and alveolar bone loss approximately threefold when compared to nondiabetic control subjects. These findings have been confirmed in meta-analyses of multiple studies in various diabetic populations. Diabetes increases not only the prevalence and severity of periodontitis but also the progression of bone loss and attachment loss over time.
Periodontitis is similar to the classic complications of diabetes in its variation among individuals. Just as retinopathy, nephropathy, and neuropathy are more likely to be seen in diabetic patients with poor glycemic control, progressive destructive periodontitis is also more common in those with poor control. However, some poorly controlled diabetic patients do not develop significant periodontal destruction, just as some do not develop the classic diabetic complications. Conversely, well-controlled diabetes places the person at a lower risk for periodontal disease, similar to the risk of nondiabetic individuals; yet, well-controlled diabetic patients may still develop periodontitis, just as nondiabetic individuals do. Other risk factors for periodontitis, such as poor oral hygiene and smoking, play a similar deleterious role in both diabetic and nondiabetic individuals.
The mechanisms by which diabetes influences the periodontium are similar in many respects to the pathophysiology of the classic diabetic complications. There are few differences between the subgingival microbiota of diabetic patients with periodontitis and nondiabetic patients with periodontitis. This lack of significant differences in the primary bacteriologic agents of periodontal disease suggests that differences in host response may play a role in the increased prevalence and severity of periodontal destruction seen in patients with diabetes.
Hyperglycemia results in increased gingival crevicular fluid glucose levels, which may significantly alter periodontal wound-healing events by changing the interaction between cells and their extracellular matrix within the periodontium. Vascular changes seen in the retina, glomerulus, and perineural areas also occur in the periodontium. The formation of AGEs results in collagen accumulation in the periodontal capillary basement membranes, causing membrane thickening. AGE-stimulated smooth-muscle proliferation increases the thickness of vessel walls. These changes decrease tissue perfusion and oxygenation. AGE-modified collagen in gingival blood vessel walls binds circulating LDL, which is frequently elevated in diabetes, resulting in atheroma formation and further narrowing of the vessel lumen. These changes in the periodontium may dramatically alter the tissue response to periodontal pathogens, resulting in increased tissue destruction and diminished repair potential.
The Hypoglycemic States
Spontaneous hypoglycemia in adults is of two principal types: fasting and postprandial. Symptoms begin ...
Diabetes results in changes in the function of host defense cells such as polymorphonuclear leukocytes (PMNs), monocytes, and macrophages. PMN adherence, chemotaxis, and phagocytosis are impaired. Defects in this first line of defense against periodontopathic microorganisms may significantly increase periodontal destruction. Monocytes and macrophages in diabetic individuals are often hyper-responsive to bacterial antigens.65 This up-regulation results in a significantly increased production of proinflammatory cytokines and mediators. The net effect of these host defense alterations is an increase in periodontal inflammation, attachment loss, and bone loss.
Gum Disease Signs
Plaque is the main cause of gum disease, but diabetes can also be a culprit because it may weaken your mouth's germ-fighting powers. High blood glucose levels can make gum disease worse, and at the same time, gum disease can make diabetes harder to control.
Often gum disease is painless. You may not even know you have it until you have some serious damage. Regular dentist visits are your best weapon.
While gum disease may not hurt, there are warning signs to watch for.
- Bleeding gums when you brush or floss. This bleeding is not normal. Even if your gums don't hurt, get them checked.
- Red, swollen or tender gums
- Gums that have pulled away from teeth. Part of the tooth's root may show, or your teeth may look longer.
- Pus between the teeth and gums (when you press on the gums)
- Bad breath
- Permanent teeth that are loose or moving away from each other
- Changes in the way your teeth fit when you bite
- Changes in the fit of partial dentures or bridges
Collagen is the primary structural protein in the periodontium. Changes in collagen metabolism in diabetic individuals contribute to wound-healing alterations and periodontal destruction. The production of matrix metalloproteinases (MMPs) such as collagenase is increased in many diabetic patients. Increased collagenase production readily degrades newly formed collagen. Conversely, AGE modification of existing collagen decreases its solubility. The result of these changes in collagen metabolism is a rapid dissolution of recently synthesized collagen by host collagenase and a preponderance of older AGE-modified collagen. Thus, diabetes induces a shift in the normal homeostatic mechanism by which collagen is formed, stabilized, and eventually turned over; this shift alters healing responses to physical or microbial wounding of the periodontium. Tetracycline antibiotics and chemically modified tetracycline agents reduce host collagenase production and collagen degradation through mechanisms that are independent of their antimicrobial activity. These drugs may have benefits in managing conditions such as periodontitis, arthritis, diabetes, osteoporosis, and others in which collagen metabolism is altered.
Periodontal Risk Factors and Indicators
The American Academy of Periodontology (AAP) has established a protocol toward standardizing a comprehensive approach in the assessment, diagnosis and treatment of periodontitis associated with systemic conditions. The imperative implication of this parameter is to ensure that patients are informed about the significance of their systemic condition(s) and the probable impact it can have to the periodontal disease process. A conscientious effort should be made in presenting therapeutic choices and alternatives, potential complications, and expected outcomes. An informed patient has a thorough understanding of their rights and responsibilities as an active participant in the treatment decision, applications and successful outcomes within their periodontal therapy or in declining to proceed with the prescribed treatment.
It is important to consider periodontal risk factors because they can affect periodontal disease onset, progression and severity. Risk factors include genetics, ethnicity, advancing age, smoking, diabetes, specific medications, impaired nutrition, poor oral hygiene, poor dental restorations, hormonal variations, immunocompromised status, connective tissue diseases and previous history of periodontal disease.
A comprehensive periodontal evaluation should include a review of systemic disorders, oral signs and symptoms, medication history, addictive habits, familial factors, psychological issues and disease states. Signs and symptoms of undiagnosed or poorly controlled diabetes need to be identified. Consultation with the patient's physician should be included and deemed necessary. The patient should receive instructions on medications and diet during periodontal therapy as well as education regarding the possible impact of periodontal infection on their glycemic control. The office needs to be prepared to manage diabetic and other medical emergencies.
Effect of Uncontrolled Periodontal Disease on Diabetes Mellitus
Severe periodontal disease often coexists with severe diabetes and the converse possibility that periodontal disease either predisposes or exacerbates the diabetic condition is in the forefront of current research. A link has been proposed that a rise in proinflammatory cytokines (proteins regulating the intensity and duration of the immune response) stimulates secretions from periodontopathic organisms that may amplify the impact on the metabolic state of the diabetic patient. This reaction can reduce glycemic control, affect insulin resistance and increase the risk of developing other diabetic complications.
Studies suggest a plausible link on periodontitis to the affect and pathogenesis of systemic diseases through inflammatory changes that are elicited from the onset, fuelling a chronic infection especially where periodontal treatment is lacking. Researchers will continue seeking evidence to define the virulence and invasiveness of periodontal disease by its mechanism of putting stress on the body through spreading bacteria, increasing the inflammatory burden, or both.
Impact of Periodontal Treatment on Diabetes
More research is emerging that suggests a bidirectional relationship between both types of diabetes and periodontal disease: the body responds to severe periodontitis with an increased blood glucose level, while periodontitis makes it more difficult for the diabetic to control their blood glucose level. It is accepted that the removal of periodontal pathogens can slow or arrest the progression of periodontitis by reducing local inflammation. However, the diabetic patient, being at a greater risk of developing periodontitis due to impaired immune responses, may not respond as well to periodontal therapy as a non-diabetic patient. An hypothesis on the basis of a direct inflammation theory in linking oral disease to systemic health is that serum levels of inflammatory mediators that cause insulin resistance may be reduced through periodontal therapies, which may improve glycemic control.
A conclusive meta-analysis by Janket et al revealed that periodontal treatment does not affect glycemic control by reducing A1C levels in diabetic patients, but recognized that the study designs impacted on the results. The variety of periodontal treatments (non-surgical with and without antibiotics) and unbalanced population samples (type 1, type 2 or mixed) lend to conflicting results, and it was therefore strongly recommended that further studies, possibly restricted to type 2 diabetics not on insulin regimens, could more accurately demonstrate the significant effects of periodontal therapies on glycemic controls in diabetics.
Further rigorous and controlled studies of the treatment of periodontal disease in diabetics are needed to confirm the extent to which treatment enhances glycemic control. However, there is evidence that well-controlled diabetics respond to periodontal therapies similarly as non-diabetics and diabetics continually challenged may have a less favorable outcome over the long term.
Oral Complications and Manifestations of Diabetes Mellitus
Several soft tissue abnormalities have been reported to be associated with diabetes mellitus in the oral cavity. These complications include periodontal diseases (periodontitis and gingivitis); salivary dysfunction leading to a reduction in salivary flow and changes in saliva composition, and taste dysfunction. Oral fungal and bacterial infections have also been reported in patients with diabetes. There are also reports of oral mucosa lesions in the form of stomatitis, geographic tongue, benign migratory glossitis, fissured tongue, traumatic ulcer, lichen planus, lichenoid reaction and angular chelitis. In addition, delayed mucosal wound healing, mucosal neuro-sensory disorders, dental carries and tooth loss has been reported in patients with diabetes. The prevalence and the chance of developing oral mucosal lesions were found to be higher in patients with diabetes compared to healthy controls.
Periodontal Diseases
Periodontitis is one of the most widespread diseases in the world affecting the oral cavity, and is highly prevalent in both developed and developing countries. Periodontitis is a chronic inflammatory disorder affecting the gingivae and the periodontal tissue initiated by bacteria. The micro-flora in the dental plaque that forms daily adjacent to the teeth causes this inflammatory process. Eventually, the toxins that are released by the microorganisms in the dental plaque will start the gingival inflammation as a result of failure to remove the dental plaque on a daily basis. A periodontal pocket is formed as a result of the progression of the gingival inflammation causing the gingivae to detach from the tooth surface. This periodontal pocket is filled with bacteria and its toxins. As the disease worsens, the pocket will get deeper carrying the dental plaque until it reaches the alveolar bone that will eventually be destroyed with the periodontal attachment. This process is very common and causes destruction of periodontal tissues, loss of alveolar bone and, finally, tooth loss. There are many factors contributing to this type of inflammation beside the presence of bacteria in dental plaque; a susceptible host is one of them.
Periodontitis and Diabetes Mellitus
The link between diabetes mellitus and periodontal disease is not well recognised by the medical community. Periodontal disease has been reported with increased prevalence and severity in patients with type 1 and type 2 diabetes. The mechanism by which hyperglycaemia can induce periodontal destruction is not yet fully understood. However, there are many theories which propose factors such as advanced glycation end products, changes in collagen statue, and altered immune function that causes impaired polymorphonuclear leukocyte function which may facilitate bacterial persistence in the tissue and the accumulation of advanced glycation end products, which results from prolonged and chronic hyperglycaemia and increased secretion of pro-inflammatory cytokines such as tumour necrosis factor-α and prostaglandin E-2. The increase in collagenase activity together with the reduction in collagen synthesis will adversely influence collagen metabolism. This would result in compromised wound healing as well as periodontal tissue destruction. Recent studies indicate that periodontitis has a bidirectional effect on glycaemic control in patients with diabetes. There is a cluster of research studies, which support the hypothesis of periodontitis occurring more frequently in patients with diabetes with poor glycaemic control. In addition, there is enough evidence to support the hypothesis that poor periodontal conditions could worsen glycaemic control as well. Many studies report that diabetes is a risk factor for gingivitis and periodontitis and it is more severe with poor glycaemic control. The risk of developing periodontitis in patients with diabetes has been reported to be three times higher than the general population.
Numerous risk factors have been reported that make patients with diabetes more susceptible to periodontal disease, especially those with poor oral hygiene, poor metabolic control, longer duration of diabetes and who are smokers. Smoking was identified in many studies as being a major preventable risk factor for periodontal disease and tooth loss in the general population and in patients with diabetes. The dentist and the physician should play an important role in advising and supporting patients with diabetes regarding smoking cessation. The dentist should be engaged in counselling these patients and referring them to a specialist organisation which deals with smoking cessation.
Conclusion
Diabetes mellitus is a metabolic condition affecting multiple organ systems. The oral cavity frequently undergoes changes that are related to the diabetic condition, and oral infections may adversely affect metabolic control of the diabetic state. The mechanisms underlie the oral effects of diabetes share many similarities with the mechanisms that are responsible for the classic diabetic complications. The intimate relationship between oral health and systemic health in individuals with diabetes suggests a need for increased interaction between the dental and medical professionals who are charged with the management of these patients. Oral health assessment and treatment should become as common as the eye, foot, and kidney evaluations that are routinely performed as part of preventive medical therapies. Dental professionals with a thorough understanding of current medical treatment regimens and the implications of diabetes on dental care are able to help their diabetic patients achieve and maintain the best possible oral health.
